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Baicalin suppresses the migration and invasion of breast cancer cells via the TGF-β/lncRNA-MALAT1/miR-200c signaling pathway

Metastasis is the major cause of death and failure of cancer chemotherapy in patients with breast cancer (BC). Activation of TGF-β/lncRNA-MALAT1/miR-200c has been reported to play an essential role during the metastasis of BC cells. The present study aimed to validate the suppression of BC-cell migr...

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Detalles Bibliográficos
Autores principales: Li, Jiafeng, Liu, Huixin, Lin, Qiwang, Chen, Huajiao, Liu, Liya, Liao, Hongjuan, Cheng, Ying, Zhang, Xiuli, Wang, Zhenlong, Shen, Aling, Chen, Guolong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Lippincott Williams & Wilkins 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9678613/
https://www.ncbi.nlm.nih.gov/pubmed/36401368
http://dx.doi.org/10.1097/MD.0000000000029328
Descripción
Sumario:Metastasis is the major cause of death and failure of cancer chemotherapy in patients with breast cancer (BC). Activation of TGF-β/lncRNA-MALAT1/miR-200c has been reported to play an essential role during the metastasis of BC cells. The present study aimed to validate the suppression of BC-cell migration and invasion by baicalin and explore its regulatory effects on the TGF-β/lncRNA-MALAT1/miR-200c signaling pathway. We found that baicalin treatment inhibited cell viability and migration and invasion. Mechanistically, baicalin treatment significantly downregulated the expression of TGF-β, ZEB1, and N-cadherin and upregulated E-cadherin on both mRNA and protein levels. Additionally, baicalin treatment significantly downregulated the expression of lncRNA-MALAT1 and upregulated that of miR-200c. Collectively, baicalin significantly suppresses cell viability, migration, and invasion of BC cells possibly by regulating the TGF-β/lncRNA-MALAT1/miR-200c pathway.